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Autologous faecal microbiota transplantation for type 1 diabetes: a potential mindshift in therapeutic microbiome manipulation?
  1. Gianluca Ianiro1,2,
  2. Antonio Gasbarrini1,2,
  3. Giovanni Cammarota1,2
  1. 1 Digestive Disease Center, Policlinico Universitario Agostino Gemelli IRCCS, Roma, Lazio, Italy
  2. 2 Dipartimento Universitario di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Facoltà di Medicina e Chirurgia, Roma, Lazio, Italy
  1. Correspondence to Dr Gianluca Ianiro, Digestive Disease Center, Policlinico Universitario Agostino Gemelli IRCCS, Dipartimento Universitario di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Roma, Italy; gianluca.ianiro{at}

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A growing body of evidence shows that the alteration of gut microbiota is involved in the pathogenesis of both autoimmune and metabolic disorders. This connection is straightforward, as human gut microbiota is known to shape the immune system and regulate the metabolism during early life, so its imbalance is expected to breach the homoeostatic healthy state and be a potential driver of disease. Based on this background, the increasing prevalence of both autoimmune and metabolic disorders worldwide has been hypothesised to be potentially caused by the progressive depletion of human gut microbiota that are associated with modern Western lifestyle.1 More specifically, this intriguing evolutionary theory rests on the evidence of common mechanistic pathways of response to changes in gut microbiome, that are shared by autoimmune and metabolic diseases. The use of broad-spectrum antibiotics—which are, basically, the fastest and most detrimental driver of dysbiosis—during early life has been identified as a risk factor for the later development of both early onset IBD2 and obesity/overweight,3 in human cohorts and in elegant mouse models.3 On the other side, the therapeutic modulation of gut microbiota, mainly faecal microbiota transplantation (FMT), has brought promising results in these settings, including UC4 and metabolic syndrome (MetS).5

Type 1 diabetes (T1D) represents an interesting …

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  • Twitter @gianluca1aniro, @GiovanniCammar9

  • Contributors GI: concept and writing of the manuscript. AG and GC: critical revision of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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